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Updated: Aug 18, 2026

Pairwise Growth Competition Assay for Determining the Replication Fitness of Human Immunodeficiency Viruses
Published on: May 4, 2015
Viral growth, origin binding, and p53 binding properties of simian virus 40 large T antigen transformation and
J E Rutila1, J B Christensen, M J Imperiale
1Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor 48109-0620.
Abstract:
The viability, p53 binding, and SV40 origin binding of a series of SV40 large T antigen point mutants, which map to the amino terminal one-third of the molecule, were examined. Two mutants which yield small plaques were found to have altered kinetics of replication upon infection of permissive cells. Mutants which did not bind to the origin of replication were not able to replicate, but the reverse was not always true. Replication defective mutants which bound the SV40 origin were found; these map both inside and outside of the origin binding domain. All the transformation defective mutants bound the cellular protein, p53.
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